Why does it make good metabolic sense for phosphoenolpyruvate carboxykinase, rather than
pyruvate carboxylase, to be the primary target for regulation of gluconeogenesis at the level of control
of enzyme synthesis?
Because the synthesis of phosphoenolpyruvate carboxykinase is reduced under the action of insulin, and consequently, the intensity of gluconeogenesis. Such regulation of synthesis occurs at the gene level.
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